Repression of host RNA polymerase II transcription by herpes simplex virus type 1

Charlotte A. Spencer, Michael E. Dahmus, Stephen A. Rice

Research output: Contribution to journalArticle

75 Scopus citations

Abstract

Lytic infection of mammalian cells with herpes simplex virus type 1 (HSV-1) results in rapid repression of host gene expression and selective activation of the vital genome. This transformation in gene expression is thought to involve repression of host transcription and diversion of the host RNA polymerase (RNAP II) transcription machinery to the vital genome. However, the extent of virus-induced host transcription repression and the mechanisms responsible for these major shifts in transcription specificities have not been examined. To determine how HSV-1 accomplishes repression of host RNAP II transcription, we assayed transcription patterns on several cellular genes in cells infected with mutant and wild-type HSV-1. Our results suggest that HSV-1 represses RNAP II transcription on most cellular genes. However, each cellular gene we examined responds differently to the transcription repressive effects of virus infection, both quantitatively and with respect to the involvement of vital gene products. Virus-induced shutoff of host RNAP II transcription requires expression of multiple immediate- early genes. In contrast, expression of delayed-early and late genes and vital DNA replication appear to contribute little to repression of host cell RNAP II transcription. Modification of RNAP II to the intermediately phosphorylated (II(I)) form appears unlinked to virus-induced repression of host cell transcription. However, full repression of host transcription is correlated with depletion of the hyperphosphorylated (IIO) form of RNAP II.

Original languageEnglish (US)
Pages (from-to)2031-2040
Number of pages10
JournalJournal of virology
Volume71
Issue number3
DOIs
StatePublished - Mar 1997

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